用青霉胺治疗的类风湿关节炎患者的血栓动力学
Thrombokinetics in patients with rheumatoid arthritis treated with D-penicillamine.
作者信息
Thomas D, Gallus A S, Brooks P M, Tampi R, Geddes R, Hill W
出版信息
Ann Rheum Dis. 1984 Jun;43(3):402-6. doi: 10.1136/ard.43.3.402.
The mechanism of D-penicillamine induced thrombocytopenia in rheumatoid arthritis was investigated by measuring platelet life-span and platelet production rate in 2 groups of rheumatoid arthritis patients treated with 250-750 mg/day D-penicillamine, 14 with a normal platelet count and 9 with thrombocytopenia (platelet count 50-130 X 10(9)/1). Age matched control patients not treated with D-penicillamine included 14 with rheumatoid arthritis and 9 with osteoarthritis. The platelet life-span was normal, but platelet production rate was significantly reduced in the thrombocytopenic patients, suggesting that D-penicillamine causes thrombocytopenia through bone marrow suppression.
通过测量两组类风湿性关节炎患者的血小板寿命和血小板生成率，对青霉胺诱导类风湿性关节炎患者血小板减少的机制进行了研究。这两组患者每日服用250 - 750毫克青霉胺，其中14例血小板计数正常，9例有血小板减少症（血小板计数为50 - 130×10⁹/升）。未接受青霉胺治疗、年龄匹配的对照患者包括14例类风湿性关节炎患者和9例骨关节炎患者。血小板寿命正常，但血小板减少症患者的血小板生成率显著降低，这表明青霉胺通过骨髓抑制导致血小板减少。
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